Добірка наукової літератури з теми "HCMEC"
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Статті в журналах з теми "HCMEC"
1
Zakrzewicz, A., M. Gräfe, D. Terbeek, M. Bongrazio, W. Auch-Schwelk, B. Walzog, K. Graf, E. Fleck, K. Ley, and P. Gaehtgens. "L-Selectin–Dependent Leukocyte Adhesion to Microvascular But Not to Macrovascular Endothelial Cells of the Human Coronary System." Blood 89, no. 9 (May 1, 1997): 3228–35. http://dx.doi.org/10.1182/blood.v89.9.3228.
Повний текст джерелаАнотація:
Abstract To characterize L-selectin–dependent cell adhesion to human vascular endothelium, human cardiac microvascular endothelial cells (HCMEC) and human coronary endothelial cells (HCEC) were isolated from explanted human hearts. The adhesion behavior of human (NALM-6) and mouse (300.19) pre-B cells transfected with cDNA encoding for human L-selectin was compared with that of the respective nontransfected cells in a flow chamber in vitro. More than 80% of the adhesion to tumor necrosis factor-α (TNF-α)–stimulated HCMEC at shear stresses <2 dyne/cm2 was L-selectin dependent and could be equally well blocked by an anti–L-selectin antibody or a L-selectin-IgG-chimera. No L-selectin dependent adhesion to HCEC could be shown. The L-selectin dependent adhesion to HCMEC was insensitive to neuraminidase, but greatly inhibited by addition of NaClO3 , which inhibits posttranslational sulfation and remained elevated for at least 24 hours of stimulation. E-selectin dependent adhesion of HL60 cells to HCMEC was blocked by neuraminidase, but not by NaClO3 and returned to control levels within 18 hours of HCMEC stimulation. It is concluded that microvascular, but not macrovascular endothelial cells express TNF-α–inducible sulfated ligand(s) for L-selectin, which differ from known L-selectin ligands, because sialylation is not required. The prolonged time course of L-selectin dependent adhesion suggests a role in sustained leukocyte recruitment into inflammatory sites in vivo.
2
Marquez-Curtis, Leah A., Reid Bokenfohr, Locksley E. McGann, and Janet A. W. Elliott. "Cryopreservation of human cerebral microvascular endothelial cells and astrocytes in suspension and monolayers." PLOS ONE 16, no. 4 (April 14, 2021): e0249814. http://dx.doi.org/10.1371/journal.pone.0249814.
Повний текст джерелаАнотація:
The blood–brain barrier (BBB) keeps pathogens and toxins out of the brain but also impedes the entry of pharmaceuticals. Human cerebral microvascular endothelial cells (hCMECs) and astrocytes are the main functional cell components of the BBB. Although available commercially as cryopreserved cells in suspension, improvements in their cryopreservation and distribution as cryopreserved monolayers could enhance BBB in vitro studies. Here, we examined the response to slow cooling and storage in liquid nitrogen of immortalized hCMEC/D3 cells and human primary astrocytes in suspension and in monolayers. HCMEC/D3 cells in suspension cryopreserved in 5% dimethyl sulfoxide (DMSO) and 95% fetal bovine serum or in 5% DMSO and 6% hydroxyethyl starch (HES) showed post-thaw membrane integrities above 90%, similar to unfrozen control. Cryopreservation did not affect the time-dependent ability of hCMEC/D3 cells to form tubes on Matrigel. Primary astrocytes in suspension cryopreserved in the presence of 5% DMSO and 6% HES had improved viability over those cryopreserved in 10% DMSO. Monolayers of single cultures or co-cultures of hCMEC/D3 cells and astrocytes on fibronectin-coated Rinzl coverslips retained membrane integrities and metabolic function, after freezing in 5% DMSO, 6% HES, and 2% chondroitin sulfate, that were comparable to those of unfrozen controls even after overnight incubation. Rinzl is better than glass or Thermanox as an underlying solid substrate for cryopreserving hCMEC/D3 monolayers. Cryopreserved hCMEC/D3 monolayers expressed the junction proteins ZO-1 and claudin-5 similar to their unfrozen counterparts. Hence, we describe improved cryopreservation protocols for hCMEC/D3 cells and astrocytes in suspension, and a novel protocol for the cryopreservation of monolayers of hCMEC/D3 cells and astrocytes as single cultures or co-cultures that could expand their distribution for research on disease modeling, drug screening, and targeted therapy pertaining to the BBB.
3
Meli, Athinoula, Ann McCormack, Ianina Conte, Qu Chen, James Streetley, Marlene L. Rose, Ruben Bierings, et al. "Altered Storage and Function of von Willebrand Factor in Human Cardiac Microvascular Endothelial Cells Isolated from Recipient Transplant Hearts." International Journal of Molecular Sciences 24, no. 5 (February 25, 2023): 4553. http://dx.doi.org/10.3390/ijms24054553.
Повний текст джерелаАнотація:
The assembly of von Willebrand factor (VWF) into ordered helical tubules within endothelial Weibel–Palade bodies (WPBs) is required for the efficient deployment of the protein at sites of vascular injury. VWF trafficking and storage are sensitive to cellular and environmental stresses that are associated with heart disease and heart failure. Altered storage of VWF manifests as a change in WPB morphology from a rod shape to a rounded shape and is associated with impaired VWF deployment during secretion. In this study, we examined the morphology, ultrastructure, molecular composition and kinetics of exocytosis of WPBs in cardiac microvascular endothelial cells isolated from explanted hearts of patients with a common form of heart failure, dilated cardiomyopathy (DCM; HCMECD), or from nominally healthy donors (controls; HCMECC). Using fluorescence microscopy, WPBs in HCMECC (n = 3 donors) showed the typical rod-shaped morphology containing VWF, P-selectin and tPA. In contrast, WPBs in primary cultures of HCMECD (n = 6 donors) were predominantly rounded in shape and lacked tissue plasminogen activator (t-PA). Ultrastructural analysis of HCMECD revealed a disordered arrangement of VWF tubules in nascent WPBs emerging from the trans-Golgi network. HCMECD WPBs still recruited Rab27A, Rab3B, Myosin-Rab Interacting Protein (MyRIP) and Synaptotagmin-like protein 4a (Slp4-a) and underwent regulated exocytosis with kinetics similar to that seen in HCMECc. However, secreted extracellular VWF strings from HCMECD were significantly shorter than for endothelial cells with rod-shaped WPBs, although VWF platelet binding was similar. Our observations suggest that VWF trafficking, storage and haemostatic potential are perturbed in HCMEC from DCM hearts.
4
Omatsu, Tatsushi, Gediminas Cepinskas, Cheril Clarson, Eric K. Patterson, Ibrahim M. Alharfi, Kelly Summers, Pierre-Olivier Couraud, Ignacio A. Romero, Babette Weksler та Douglas D. Fraser. "CXCL1/CXCL8 (GROα/IL-8) in human diabetic ketoacidosis plasma facilitates leukocyte recruitment to cerebrovascular endothelium in vitro". American Journal of Physiology-Endocrinology and Metabolism 306, № 9 (1 травня 2014): E1077—E1084. http://dx.doi.org/10.1152/ajpendo.00659.2013.
Повний текст джерелаАнотація:
Diabetic ketoacidosis (DKA) in children is associated with intracranial vascular complications, possibly due to leukocyte-endothelial interactions. Our aim was to determine whether DKA-induced inflammation promoted leukocyte adhesion to activated human cerebrovascular endothelium. Plasma was obtained from children with type 1 diabetes either in acute DKA or in an insulin-controlled state (CON). Plasma concentrations of 21 inflammatory analytes were compared between groups. DKA was associated with altered circulating levels of ↑CXCL1 (GROα), ↑CXCL8 (IL-8), ↑IL-6, ↑IFNα2, and ↓CXCL10 (IP-10) compared with CON. These plasma analyte measurements were then used to create physiologically relevant cytokine mixtures (CM). Human cerebral microvascular endothelial cells (hCMEC/D3) were stimulated with either plasma (DKA-P or CON-P) or CM (DKA-CM or CON-CM) and assessed for polymorphonuclear leukocyte (PMN) adhesion. Stimulation of hCMEC/D3 with DKA-P or DKA-CM increased PMN adhesion to hCMEC/D3 under “flow” conditions. PMN adhesion to hCMEC/D3 was suppressed with neutralizing antibodies to CXCL1/CXCL8 or their hCMEC/D3 receptors CXCR1/CXCR2. DKA-P, but not DKA-CM, initiated oxidative stress in hCMEC/D3. Expression of ICAM-1, VCAM-1, and E-selectin were unaltered on hCMEC/D3 by either DKA-P or DKA-CM. In summary, DKA elicits inflammation in children associated with changes in circulating cytokines/chemokines. Increased CXCL1/CXCL8 instigated PMN adhesion to hCMEC/D3, possibly contributing to DKA-associated intracranial vascular complications.
5
Khalyfa, Abdelnaby, David Gozal, and Leila Kheirandish-Gozal. "Plasma Extracellular Vesicles in Children with OSA Disrupt Blood–Brain Barrier Integrity and Endothelial Cell Wound Healing In Vitro." International Journal of Molecular Sciences 20, no. 24 (December 10, 2019): 6233. http://dx.doi.org/10.3390/ijms20246233.
Повний текст джерелаАнотація:
Pediatric obstructive sleep apnea (P-OSA) is associated with neurocognitive deficits and endothelial dysfunction, suggesting the possibility that disruption of the blood–brain barrier (BBB) may underlie these morbidities. Extracellular vesicles (EVs), which include exosomes, are small particles involved in cell–cell communications via different mechanisms and could play a role in OSA-associated end-organ injury. To examine the roles of EVs in BBB dysfunction, we recruited three groups of children: (a) absence of OSA or cognitive deficits (CL, n = 6), (b) OSA but no evidence of cognitive deficits (OSA-NC(−), n = 12), and (c) OSA with evidence of neurocognitive deficits (OSA-NC(+), n = 12). All children were age-, gender-, ethnicity-, and BMI-z-score-matched, and those with OSA were also apnea–hypopnea index (AHI)-matched. Plasma EVs were characterized, quantified, and applied on multiple endothelial cell types (HCAEC, HIAEC, human HMVEC-D, HMVEC-C, HMVEC-L, and hCMEC/D3) while measuring monolayer barrier integrity and wound-healing responses. EVs from OSA children induced significant declines in hCMEC/D3 transendothelial impedance compared to CL (p < 0.001), and such changes were greater in NC(+) compared to NC(−) (p < 0.01). The effects of EVs from each group on wound healing for HCAEC, HIAEC, HMVED-d, and hCMEC/D3 cells were similar, but exhibited significant differences across the three groups, with evidence of disrupted wound healing in P-OSA. However, wound healing in HMVEC-C was only affected by NC(+) (p < 0.01 vs. NC(−) or controls (CO). Furthermore, no significant differences emerged in HMVEC-L cell wound healing across all three groups. We conclude that circulating plasma EVs in P-OSA disrupt the integrity of the BBB and exert adverse effects on endothelial wound healing, particularly among OSA-NC(+) children, while also exhibiting endothelial cell type selectivity. Thus, circulating EVs cargo may play important roles in the emergence of end-organ morbidity in pediatric OSA.
6
Samak, Mostafa, Diana Kaltenborn, Andreas Kues, Ferdinand Le Noble, Rabea Hinkel, and Giulia Germena. "Micro-RNA 92a as a Therapeutic Target for Cardiac Microvascular Dysfunction in Diabetes." Biomedicines 10, no. 1 (December 28, 2021): 58. http://dx.doi.org/10.3390/biomedicines10010058.
Повний текст джерелаАнотація:
Microvascular dysfunction is a pathological hallmark of diabetes, and is central to the ethology of diabetes-associated cardiac events. Herein, previous studies have highlighted the role of the vasoactive micro-RNA 92a (miR-92a) in small, as well as large, animal models. In this study, we explore the effects of miR-92a on mouse and human cardiac microvascular endothelial cells (MCMEC, HCMEC), and its underlying molecular mechanisms. Diabetic HCMEC displayed impaired angiogenesis and a pronounced inflammatory phenotype. Quantitative PCR (qPCR) showed an upregulation of miR-92a in primary diabetic HCMEC. Downregulation of miR-92a by antagomir transfection in diabetic HCMEC rescued angiogenesis and ameliorated diabetic endothelial bed inflammation. Furthermore, additional analysis of potential in silico-identified miR-92a targets in diabetic HCMEC revealed the miR-92a dependent downregulation of an essential metalloprotease, ADAM10. Accordingly, downregulation of ADAM10 impaired angiogenesis and wound healing in MCMEC. In myocardial tissue slices from diabetic pigs, ADAM10 dysregulation in micro- and macro-vasculature could be shown. Altogether, our data demonstrate the role of miR-92a in cardiac microvascular dysfunction and inflammation in diabetes. Moreover, we describe for the first time the metalloprotease ADAM10 as a novel miR-92a target, mediating its anti-angiogenic effect.
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Roig-Carles, David, Eduard Willms, Ruud D. Fontijn, Sarai Martinez-Pacheco, Imre Mäger, Helga E. de Vries, Mark Hirst, et al. "Endothelial-Derived Extracellular Vesicles Induce Cerebrovascular Dysfunction in Inflammation." Pharmaceutics 13, no. 9 (September 21, 2021): 1525. http://dx.doi.org/10.3390/pharmaceutics13091525.
Повний текст джерелаАнотація:
Blood–brain barrier (BBB) dysfunction is a key hallmark in the pathology of many neuroinflammatory disorders. Extracellular vesicles (EVs) are lipid membrane-enclosed carriers of molecular cargo that are involved in cell-to-cell communication. Circulating endothelial EVs are increased in the plasma of patients with neurological disorders, and immune cell-derived EVs are known to modulate cerebrovascular functions. However, little is known about whether brain endothelial cell (BEC)-derived EVs themselves contribute to BBB dysfunction. Human cerebral microvascular cells (hCMEC/D3) were treated with TNFα and IFNy, and the EVs were isolated and characterised. The effect of EVs on BBB transendothelial resistance (TEER) and leukocyte adhesion in hCMEC/D3 cells was measured by electric substrate cell-substrate impedance sensing and the flow-based T-cell adhesion assay. EV-induced molecular changes in recipient hCMEC/D3 cells were analysed by RT-qPCR and Western blotting. A stimulation of naïve hCMEC/D3 cells with small EVs (sEVs) reduced the TEER and increased the shear-resistant T-cell adhesion. The levels of microRNA-155, VCAM1 and ICAM1 were increased in sEV-treated hCMEC/D3 cells. Blocking the expression of VCAM1, but not of ICAM1, prevented sEV-mediated T-cell adhesion to brain endothelia. These results suggest that sEVs derived from inflamed BECs promote cerebrovascular dysfunction. These findings may provide new insights into the mechanisms involving neuroinflammatory disorders.
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Cucullo, Luca, Pierre-Olivier Couraud, Babette Weksler, Ignacio-Andres Romero, Mohammed Hossain, Edward Rapp, and Damir Janigro. "Immortalized Human Brain Endothelial Cells and Flow-Based Vascular Modeling: A Marriage of Convenience for Rational Neurovascular Studies." Journal of Cerebral Blood Flow & Metabolism 28, no. 2 (July 4, 2007): 312–28. http://dx.doi.org/10.1038/sj.jcbfm.9600525.
Повний текст джерелаАнотація:
In evaluating drugs that enter or are excluded from the brain, novel pharmaceutical strategies are needed. For this reason, we have developed a humanized Dynamic In vitro Blood—Brain Barrier model (hDIV-BBB) based on a novel human brain vascular endothelial cell line (HCMEC/D3), which closely mimics the BBB in vivo. In this system, HCMEC/D3 was grown in the lumen of hollow microporous fibers and exposed to a physiological pulsatile flow. Comparison with well-established humanized DIV-BBB models (based on human brain and non-brain vascular endothelial cells co-cultured with abluminal astrocytes) demonstrated that HCMEC/D3 cells cultured under flow conditions maintain in vitro physiological permeability barrier properties of the BBB in situ even in the absence of abluminal astrocytes. Measurements of glucose metabolism demonstrated that HCMEC/D3 cells retain an aerobic metabolic pathway. Permeability to sucrose and two relevant central nervous system drugs showed that the HCMEC/D3 cells grown under dynamic conditions closely mimic the physiological permeability properties of the BBB in situ (slope = 0.93). Osmotic disruption of the BBB was also successfully achieved. Peak BBB opening in the DIV-BBB lasted from 20 to 30 mins and was completely reversible. Furthermore, the sequence of flow cessation/reperfusion in the presence of leukocytes led to BBB failure as demonstrated by a biphasic decrease in transendothelial electrical resistance. Additionally, BBB failure was paralleled by the intraluminal release of proinflammatory factors (interleukin-6 and interleukin-1β) and matrix metalloproteinase-9 (MMP-9). Pretreatment with ibuprofen (0.125 mmol/L) prevented BBB failure by decreasing the inflammatory response after flow cessation/reperfusion.
9
Chen, Yanlan, Wen Huang, Wenlin Jiang, Xianghong Wu, Biao Ye та Xiaoting Zhou. "HIV-1 Tat Regulates Occludin and AβTransfer Receptor Expression in Brain Endothelial Cells via Rho/ROCK Signaling Pathway". Oxidative Medicine and Cellular Longevity 2016 (2016): 1–9. http://dx.doi.org/10.1155/2016/4196572.
Повний текст джерелаАнотація:
HIV-1 transactivator protein (Tat) has been shown to play an important role in HIV-associated neurocognitive disorders. The aim of the present study was to evaluate the relationship between occludin and amyloid-beta (Aβ) transfer receptors in human cerebral microvascular endothelial cells (hCMEC/D3) in the context of HIV-1-related pathology. The protein expressions of occludin, receptor for advanced glycation end products (RAGE), and low-density lipoprotein receptor-related protein 1 (LRP1) in hCMEC/D3 cells were examined using western blotting and immunofluorescent staining. The mRNA levels of occludin, RAGE, and LRP1 were measured using quantitative real-time polymerase chain reaction. HIV-1 Tat at 1 µg/mL and the Rho inhibitor hydroxyfasudil (HF) at 30 µmol/L, with 24 h exposure, had no significant effect on hCMEC/D3 cell viability. Treatment with HIV-1 Tat protein decreased mRNA and protein levels of occludin and LRP1 and upregulated the expression of RAGE; however, these effects were attenuated by HF. These data suggest that the Rho/ROCK signaling pathway is involved in HIV-1 Tat-mediated changes in occludin, RAGE, and LRP1 in hCMEC/D3 cells. HF may have a beneficial influence by protecting the integrity of the blood-brain barrier and the expression of Aβtransfer receptors.
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Chandrasekar, Bysani, Kirankumar Vemula, Rama Mohan Surabhi, Min Li-Weber, Laurie B. Owen-Schaub, Liselotte E. Jensen, and Srinivas Mummidi. "Activation of Intrinsic and Extrinsic Proapoptotic Signaling Pathways in Interleukin-18-mediated Human Cardiac Endothelial Cell Death." Journal of Biological Chemistry 279, no. 19 (February 11, 2004): 20221–33. http://dx.doi.org/10.1074/jbc.m313980200.
Повний текст джерелаАнотація:
Endothelial cells are the primary targets of circulating immune and inflammatory mediators. We hypothesize that interleukin-18, a proinflammatory cytokine, induces endothelial cell apoptosis. Human cardiac microvascular endothelial cells (HCMEC) were treated with interleukin (IL) 18. mRNA expression was analyzed by ribonuclease protection assay, protein levels by immunoblotting, and cell death by enzyme-linked immunosorbent assay and fluorescence-activated cell sorter analysis. We also investigated the signal transduction pathways involved in IL-18-mediated cell death. Treatment of HCMEC with IL-18 increases 1) NF-κB DNA binding activity; 2) induces κB-driven luciferase activity; 3) induces IL-1β and TNF-α expression via NF-κB activation; 4) inhibits antiapoptotic Bcl-2 and Bcl-XL; 5) up-regulates proapoptotic Fas, Fas-L, and Bcl-XSexpression; 6) inducesfasand Fas-L promoter activities via NF-κB activation; 7) activates caspases-8, -3, -9, and BID; 8) induces cytochromecrelease into the cytoplasm; 9) inhibits FLIP; and 10) induces HCME cell death by apoptosis as seen by increased annexin V staining and increased levels of mono- and oligonucleosomal fragmented DNA. Whereas overexpression of Bcl-2 significantly attenuated IL-18-induced endothelial cell apoptosis, Bcl-2/Bcl-XLchimeric phosphorothioated 2′-MOE-modified antisense oligonucleotides potentiated the proapoptotic effects of IL-18. Furthermore, caspase-8, IKK-α, and NF-κB p65 knockdown or dominant negative IκB-α and dominant negative IκB-β or kinase dead IKK-β significantly attenuated IL-18-induced HCME cell death. Effects of IL-18 on cell death are direct and are not mediated by intermediaries such as IL-1β, tumor necrosis factor-α, or interferon-γ. Taken together, our results indicate that IL-18 activates both intrinsic and extrinsic proapoptotic signaling pathways, induces endothelial cell death, and thereby may play a role in myocardial inflammation and injury.
Дисертації з теми "HCMEC"
1
Zaum, Sebastian [Verfasser], and Carola [Gutachter] Förster. "Die hCMEC/D3-Zelllinie als humanes in-vitro-Modell der Blut-Hirn-Schranke im ischämischen Schlaganfall / Sebastian Zaum ; Gutachter: Carola Förster." Würzburg : Universität Würzburg, 2018. http://d-nb.info/1164380338/34.
Повний текст джерела
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Hinkel, Sarah Verfasser], Christel [Akademischer Betreuer] [Müller-Goymann, and Stephan [Akademischer Betreuer] Reichl. "Parametrische Untersuchung des Einflusses verschiedener Kultivierungsbedingungen auf die Barriereeigenschaften von hCMEC/D3 Zellen unter Verwendung eines dynamischen Zellkulturmodells / Sarah Hinkel ; Christel Müller-Goymann, Stephan Reichl." Braunschweig : Technische Universität Braunschweig, 2020. http://d-nb.info/1215837054/34.
Повний текст джерела
3
Jacob, Aude. "Le récepteur Aryl hydrocarbon au niveau de la barrière hémato-encéphalique : implication dans la régulation de l'expression de ABCB1, ABCG2 et du CYP1B1." Thesis, Paris 5, 2012. http://www.theses.fr/2012PA05P653.
Повний текст джерелаАнотація:
Les principaux transporteurs ABC et cytochromes P450 exprimés au niveau des microvaisseaux cérébraux chez l’homme sont l’ABCB1/P-gp, l’ABCG2/BCRP et le CYP1B1. Au niveau des organes périphériques, la régulation de l’expression de ces trois marqueurs fait intervenir des facteurs de transcription et notamment le récepteur aryl hydrocarbon (AhR). Or les transcrits d’AhR sont très exprimés au niveau des microvaisseaux cérébraux humains. Les travaux de cette thèse ont donc dans un premier temps été consacrés à l’étude de l’implication de la voie du récepteur Ah dans la régulation de l’expression de l’ABCB1, de l’ABCG2 et du CYP1B1 au niveau de la barrière hémato-encéphalique. In vivo, nous avons mis en évidence qu’un traitement aigu par la dioxine (ou TCDD), ligand puissant d’AhR, induisait l’expression génique et protéique du Cyp1b1 au niveau des microvaisseaux cérébraux de rats adultes Srague-Dawley. De même, in vitro, l’exposition au TCDD a fortement induit l’expression du CYP1B1 dans la lignée hCMEC/D3, un modèle in vitro de l’endothélium cérébral humain et le recours à la technique de l’ARN interférence nous a permis de démontrer que le récepteur Ah était impliqué dans les effets observés. En revanche, que ce soit in vivo ou in vitro, l’exposition au TCDD n’a entrainé aucune modification significative de l’expression de l’ABCB1 ou de l’ABCG2. Dans un second temps, nous avons étudié l’interrelation entre la voie AhR et les voies de réponse à l’hypoxie cellulaire. Les différentes expériences réalisées sur la lignée cellulaire hCMEC/D3 ont mis en évidence une interaction non réciproque entre ces deux voies de signalisation : en cas d’activation simultanée, la réponse à l’hypoxie abolit la réponse AhR tandis que l’activation de la voie AhR ne modifie pas la réponse adaptative à l’hypoxieABCB1 (P-gp), ABCG2 (BCRP) and CYP1B1 are the main ABC transporters and cytochrome P450 enzymes expressed at the human blood-brain barrier (BBB). In peripheral tissue, expression of these proteins is regulated by transcription factors such as the aryl hydrocarbon receptor (AhR). Interestingly, high levels of AhR mRNA are detected in human brain microvessels. We therefore investigated the potential implication of AhR in the regulation of ABCB1, ABCG2 and CYP1B1 expression. In vivo, a single dose of TCDD, a highly potent AhR ligand, increased Cyp1b1 transcripts and protein expression in rat brain microvessels. Similarly, exposing hCMEC/D3 cells, an in vitro promising model of human BBB, to TCDD induced CYP1B1 expression. Using small interfering RNA, we established AhR involvement in TCDD effects. However, either in vivo or in vitro TCDD treatment had no effect on ABCB1 or ABCG2 expression. Next, we investigated the crosstalk between AhR and hypoxia signalling pathways in case of simultaneous activation. Our experiments revealed that a crosstalk between these two pathways effectively occurred in hCMEC/D3 cells: hypoxia inhibited AhR response but not the reverse
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Sun, Ping. "Study of the role of SSAO/VAP-1 in OGD conditions using SSAO/VAP-1-expressing HUVEC and human brain endothelial cells (hCMEC/D3) as experimental models of ischemic stroke, and its possible nexus with Alzheimer´s disease." Doctoral thesis, Universitat Autònoma de Barcelona, 2015. http://hdl.handle.net/10803/308325.
Повний текст джерелаАнотація:
La proteína de adhesión vascular 1 (VAP-1) es una proteína pro-inflamatoria que facilita el reclutamiento leucocitario a través de su actividad amino oxidasa sensible a semicarbazida (SSAO, E.C 1.4.3.21). La SSAO plasmática incrementa en pacientes con infarto cerebral o “stroke” isquémico y hemorrágico, y su actividad predice la aparición de hemorragias después del tratamiento con tPA. Además, la SSAO/VAP-1 se encuentra incrementada en plasma y tejido cerebral de pacientes con enfermedad de Alzheimer (EA). Así pues, creemos que la SSAO/VAP-1 puede contribuir al daño vascular en stroke y EA. Sin embargo, los mecanismos moleculares y su posible contribución al nexo stroke-EA se desconocen.
En este trabajo hemos establecido un modelo de isquemia sencillo usando células endoteliales periféricas que expresan la SSAO/VAP-1 humana (HUVEC hSSAO/VAP-1) en condiciones de deprivación de oxígeno y glucosa (OGD). Mediante este modelo encontramos que la expresión de SSAO/VAP-1 incrementa la susceptibilidad de las células endoteliales a la OGD, y la oxidación de sus sustratos aumenta el daño vascular. Las caspasas 3 y 8 se activan durante esta muerte celular. Además, la OGD constituye un estímulo para la liberación de SSAO/VAP-1 soluble. También, una OGD corta induce la unión de leucocitos al endotelio dependiente de SSAO/VAP-1, parcialmente mediada por su actividad enzimática.
Para evaluar mejor los efectos beneficiosos de nuevos compuestos inhibidores de la actividad SSAO/VAP-1 en isquemia cerebral generamos una línea celular endotelial cerebral humana que expresa la SSAO/VAP-1 (hCMEC/D3 hSSAO/VAP-1), como modelo de barrera hematoencefálica (BHE), y establecimos también las condiciones óptimas de OGD. Mediante el uso de las células HUVEC y hCMEC/D3 que expresan SSAO/VAP-1 probamos que el DPH-4, un nuevo compuesto multidiana diseñado para la EA, es capaz de proteger ambas células y disminuir la adhesión leucocitaria dependiente de SSAO en OGD con reoxigenación (OGD-Reox). El DPH-4 también fue efectivo contra el daño inducido por OGD-Reox en presencia de beta amiloide, como modelo de patología de EA.
Para determinar los mecanismos moleculares subyacentes a los efectos beneficiosos de la simvastatina en el stroke, utilizamos las células hCMEC/D3 que expresan SSAO/VAP-1 en OGD, así como dos modelos animales de oclusión de la arteria cerebral media (MCAO). Los resultados revelaron que la simvastatina impide la liberación de SSAO/VAP-1 soluble al plasma o medio de cultivo, la cual induce la expresión de E-selectina y VCAM-1, y amplifica la inflamación y el daño subsiguiente en el cerebro infartado.
Finalmente, se estudió del posible papel de la SSAO/VAP-1 en el nexo existente entre el stroke y la EA con las células hCMEC/D3. Resultados preliminares mostraron que en las células que expresan SSAO/VAP-1, la OGD-Reox induce la expresión de BACE1 y la disminución de LRP-1, y que su sustrato es capaz de incrementar los niveles de APP. Además, el metabolismo de la metilamina por la SSAO/VAP-1 induce una muerte celular adicional cuando se co-trata con Aβ1-40D, en OGD-Reox.
De estos resultados concluimos que la expresión de SSAO/VAP-1 en endotelio puede incrementar el daño asociado a la OGD, y que la OGD induce la liberación de SSAO/VAP-1 soluble. También, que la oxidación de su sustrato media parte del daño vascular y que la adhesión leucocitaria dependiente de la SSAO/VAP-1 agrava la progresión de la patología aumentando la inflamación en isquemia. La inhibición de SSAO/VAP-1 por el DPH-4 puede aportar un beneficio terapéutico para el retraso y/o prevención del stroke, así como para su progresión a EA. La modulación de los niveles de SSAO/VAP-1 media parte de los efectos beneficiosos de la simvastatina en isquemia cerebral. Además, la presencia de SSAO/VAP-1 en el endotelio cerebral puede facilitar la generación de β-amiloide, incrementando el riesgo y el empeoramiento neurológico de la EA.Vascular adhesion protein 1 (VAP-1) is a pro-inflammatory protein that mediates leukocyte recruitment through its semicarbazide-sensitive amine oxidase (SSAO, E.C 1.4.3.21) activity. Plasmatic SSAO increases in ischemic and in hemorrhagic stroke patients, and its activity predicts the appearance of parenchymal hemorrhages after tPA treatment in ischemic stroke patients. Moreover, SSAO/VAP-1 is also increased in AD patients’ plasma and brain tissue. Hence, we believe that SSAO/VAP-1 could contribute to the vascular damage in both stroke and AD. However, the molecular mechanisms of SSAO/VAP-1 in stroke and its possible contribution to the nexus of ischemic stroke and AD have not been studied in detail. In this work, an easy ischemic model was set up by using peripheral endothelial cells expressing the human SSAO/VAP-1 protein (HUVEC hSSAO/VAP-1) under oxygen-glucose deprivation (OGD) conditions. Based on this model, it was found that SSAO/VAP-1 expression increases the susceptibility of endothelial cells to OGD, and that its substrates oxidation through its enzymatic activity increases the vascular cell damage. Caspase-3 and caspase-8 are activated during the death process. In addition, OGD constitutes a stimulus for the soluble SSAO/VAP-1 release, partly mediated by metalloproteinase-2-dependent shedding. Also, short-time OGD induces SSAO/VAP-1-dependent leukocyte binding on endothelial cells, which is partly dependent on its enzymatic activity. In order to better evaluate the beneficial effects of new pharmaceutical compounds by SSAO/VAP-1 activity inhibition under cerebral ischemia conditions, a human brain endothelial cell line expressing the human SSAO/VAP-1 (hCMEC/D3 hSSAO/VAP-1) was further generated as a model of the brain blood barrier (BBB). OGD conditions were established with these cells as well. By using hSSAO/VAP-1 HUVEC and hCMEC/D3 cells, a novel multitarget-directed ligand (MTDL) DPH-4, designed for AD therapy, was proved able to protect both endothelial cells, as well as to decrease the SSAO-dependent leukocyte adhesion under OGD with reoxygenation. DPH-4 was also effective against the damage induced by OGD and reoxygenation in the presence of beta amyloid as a model of AD pathology. With regard to determine the molecular mechanisms underlying the beneficial effect of simvastatin on ischemic stroke, hCMEC/D3 hSSAO/VAP-1 cells subjected to OGD conditions and two middle cerebral arterial occlusion (MCAO) rat models were used. Results revealed that simvastatin could suppress the release of soluble SSAO/VAP-1 into the plasma or cell culture media, which induces the expression of the adhesion molecules E-selectin and VCAM-1, and amplifies the inflammation and the consequent damage in the infarcted brain. At last, hCMEC/D3 hSSAO/VAP-1 cells were used so as to study the possible role of SSAO/VAP-1 in the nexus between ischemic stroke and AD. Preliminary results showed that in SSAO/VAP-1-expressing cells, OGD with reoxygenation induces the expression of BACE1 and decreases the expression of LRP-1, and that the substrate of SSAO/VAP-1 can further up-regulate the levels of APP under OGD with reoxygenation. Furthermore, the metabolism of methylamine by SSAO/VAP-1 activity induces additional cell death when co-treated with Aβ1-40D under OGD with reoxygenation. In summary, these results conclude that the expression of SSAO/VAP-1 in endothelial cells can increase the OGD-associated cell damage. OGD induces soluble SSAO/VAP-1 release. The oxidation of its substrate mediates part of the tissue damage. SSAO/VAP-1 activity-dependent leukocyte binding further exacerbates the disease progression by augmenting inflammation in cerebral ischemia. The inhibition of SSAO/VAP-1 activity by DPH-4 can provide a therapeutic benefit to the delay and/or prevention of ischemic stroke as well as its progression to AD. The modulation of the SSAO/VAP-1 levels mediates part of the beneficial effect of simvastatin on cerebral ischemia. In addition of ischemic condition, the presence of SSAO/VAP-1 in brain endothelium may facilitate the generation of β-amyloid, hence increasing the risk and neurological worsening of AD.
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Mertens, Charlotte Nora [Verfasser]. "Functional expression of thermo-sensitive transient receptor potential channels in cultivated human corneal endothelial cells (HCEC-12) / Charlotte Nora Mertens." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2015. http://d-nb.info/1075757304/34.
Повний текст джерела
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Brunßen, Coy. "Regulation des Transkriptionsfaktors COUP‐TFII durch Glukose und den NOTCH‐Signalweg in Endothelzellen." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2010. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-39700.
Повний текст джерелаАнотація:
Erkrankungen des Herz-Kreislaufsystems sind die häufigste Todesursache in Deutschland. Eine gestörte Funktion des Gefäßendothels spielt bei der Entstehung von Herz-Kreislauferkrankungen eine Schlüsselrolle. Das Risiko einer kardiovaskulären Erkrankung ist bei Diabetikern stark erhöht. Der Transkriptionsfaktor COUP-TFII spielt eine essentielle Rolle im Glukosemetabolismus. Gleichzeitig ist er für die Differenzierung von Endothelzellen von großer Bedeutung. Für die Differenzierung und Aufrechterhaltung des arteriellen und venösen Phänotyps von Endothelzellen sind dabei maßgeblich der NOTCH-Signalweg und insbesondere die Transkriptionsfaktoren HEY2 (arteriell) und COUP-TFII (venös) verantwortlich. Gesteigerte Glukosespiegel könnten somit Auswirkungen auf die Differenzierung von Endothelzellen haben und damit einen neuen Mechanismus für das erhöhte Risiko von Gefäßerkrankungen bei Diabetikern darstellen.
Im Rahmen der Arbeit konnte die exklusive Expression von COUP-TFII im Zellkern von humanen venösen Endothelzellen nachgewiesen werden. Humane arterielle Endothelzellen zeigten keine Expression von COUP-TFII. Außerdem konnte im Rahmen der Arbeit erstmals die spezifische Expression von COUP-TFII in humanen Endothelzellen der Koronararterie nachgewiesen werden. Die Untersuchung der COUP-TFII Promotoraktivität konnte das Expressionsmuster von COUP-TFII bestätigen. Der Promotor zeigte sowohl in den venösen Endothelzellen der humanen Nabelschnur als auch in den humanen Endothelzellen der Koronararterie Aktivität.
Die kurzzeitige Stimulation von venösen Endothelzellen mit Glukose führte zu einem starken Anstieg der COUP-TFII Expression. Eine Translokation von COUP-TFII aus dem Zellkern in das Zytoplasma konnte nicht nachgewiesen werden. Die Langzeitstimulation führte interessanterweise zu einer Verminderung der COUP-TFII Expression und zu einer Erhöhung der Expression von E-Selektin. In beiden Fällen zeigte sich keine Beeinträchtigung der Expression durch Insulin. Die durchgeführten Untersuchungen schließen eine Beteiligung des AKT-Signalweges an der Regulation aus. Es zeigte sich jedoch, dass humane venöse Endothelzellen als Insulin-sensitives Gewebe mit funktionsfähigem AKT-Signalweg einzustufen sind. Stimulationsversuche mit L-Glukose zeigten keine Regulation der COUP-TFII Expression. Eine osmotische Wirksamkeit der hohen Glukosekonzentration auf die Expression von COUP-TFII konnte somit ausgeschlossen werden. Die Deletionsanalyse des COUP-TFII Promotors konnte einen Glukose-sensitiven Bereich innerhalb des COUP-TFII Promotors identifizieren. Weiterhin konnte die Repression der Aktivität des COUP-TFII Promotors durch Hypoxie nachgewiesen werden.
Eine der wichtigen Aufgaben von Endothelzellen ist die von der endothelialen NO-Synthase (eNOS) katalysierte Bildung von Stickstoffmonoxid (NO). NO hemmt die Expression des Adhäsionsmoleküls E-Selektin. Eine verringerte NO-Produktion hat die Ausbildung einer endothelialen Dysfunktion zur Folge. In dieser Arbeit konnte erstmals eine Erhöhung der eNOS Expression nach Verminderung der Expression von COUP-TFII in humanen venösen Endothelzellen gezeigt werden. Diese könnte die Ursache für die Verminderung der E-Selektin Expression nach Herabregulation von COUP-TFII sein. Durch die Anwendung einer Plattenkegel-Viskometer-Apparatur konnte gezeigt werden, dass die NO-Abgabe entscheidend von den Strömungsbedingungen und Scherkräften abhängig ist. Die Stimulation arterieller Endothelzellen mit laminarer oder oszillatorischer Schubspannung führte zu einer Erhöhung der NO-Abgabe. Turbulente Schubspannung zeigte dagegen keinen Einfluss auf die NO-Abgabe. Durch Überexpression von COUP-TFII in Kombination mit laminarer Schubspannung wurde die NO-Abgabe weiter gesteigert. Die gezeigte direkte Regulation der HEY2 und COUP-TFII Promotoraktivität durch geänderte Strömungsbedingungen spielt in diesem Prozess möglicherweise eine bedeutende Rolle.
Die beschriebene Regulation von COUP-TFII durch Glukose in Endothelzellen könnte eine neue Erklärung für die gesteigerte Rate an Gefäßerkrankungen von Typ2-Diabetikern darstellen. Bei der Regulation der endothelialen NO-Synthase und E-Selektin durch COUP-TFII handelt es sich möglicherweise um einen neuen, anti-adhäsiven Feedback-Mechanismus, der zur Verringerung der Leukozyten-Adhäsion an Endothelzellen und damit zur Gefäßprotektion beitragen könnte.
Die differentielle Expression der arteriellen Markergene HEY2 und CD44 konnte in humanen venösen und arteriellen Endothelzellen gezeigt werden. Die Untersuchung der Expression von FOXC1 legt nahe, dass es sich bei diesem Transkriptionsfaktor ebenfalls um ein in Endothelzellen arteriovenös differentiell exprimiertes Gen handelt. Die differentielle Exprimierung von HEY2 in Endothelzellen konnte auf transkriptioneller Ebene zusätzlich durch ein HEY2 Promotor Funktionsassay gezeigt werden.
Die Überexpression der NOTCH1 intrazellulären Domäne führte zur Induktion der endogenen Expression der NOTCH-Zielgene HEY1 und HEY2 in HEK 293T Zellen. In dem Zelltyp durchgeführte Reportergenassays zeigten ebenfalls eine deutliche Aktivierung des HEY2 Promotors durch die Überexpression der NOTCH1 intrazellulären Domäne. Durch eine Deletionsanalyse konnte der Bereich, der für die Aktivierung verantwortlichen DNA-Sequenz-Motive stark eingegrenzt werden. Weiterhin konnte die Induktion des HEY2 Promotors durch VEGF und seine Repression durch einen γ-Sekretase Inhibitor nachgewiesen werden.
Die Überexpression der NOTCH1 intrazellulären Domäne führte zur Verringerung der mRNA- und Protein-Expression von COUP-TFII in HEK 293T Zellen. Dieses Ergebnis konnte zusätzlich durch ein COUP-TFII Promotor Aktivitätsassay nach Überexpression des NOTCH-Zielgens HEY2 gezeigt werden. Die Deletionsanalyse des COUP-TFII Promotors lässt eine direkte Inhibition von COUP-TFII durch HEY2 vermuten. Die Überexpression von COUP-TFII führte zu einer starken Induktion der COUP-TFII mRNA- und Protein-Expression, jedoch weder in HEK 293T Zellen noch in Endothelzellen zu einer Änderung der HEY2 Promotoraktivität.
Die Überexpression von FOXC1 und FOXC2 bewirkte eine Inhibition der HEY2 Promotoraktivität in HEK 293T Zellen. Die in der Arbeit gezeigte hohe Expression von FOXC1 in venösen Endothelzellen könnte somit in Kombination mit COUP-TFII für die komplette Repression der Aktivität des HEY2 Promotors in venösen Endothelzellen verantwortlich sein. Die durchgeführte Deletionsanalyse des HEY2 Promotors legt eine direkte Bindung von FOXC1 und FOXC2 an den HEY2 Promotor nahe.
Die erzielten Ergebnisse dieser Arbeit sprechen im Kontext mit der Literatur für eine zelltypspezifische Regulierung/Aktivierung des NOTCH-Signalweges und lassen folgendes Modell zur Differenzierung des venösen oder arteriellen endothelialen Phänotyps vermuten: Die Determinierung des Phänotyps wird entschieden durch das Gleichgewicht der Expression der Interaktionspartner des NOTCH-Signalweges. Der VEGF Co-Rezeptor NRP1 und der VEGFR2 sind die entscheidenden Aktivatoren des NOTCH-Signalweges. Die Balance der Bindung des Repressors COUP-TFII an den NRP1 und VEGFR2 Promotor sowie des Aktivatorkomplexes NICD/RBP-JК an den NRP1 Promotor sind damit entscheidend für die Aktivität des NOTCH-Signalweges. NRP1 bindet VEGF und steigert gleichzeitig dessen Bindung an den VEGFR2. Dies führt zur Induktion von DLL4. Die Bindung von DLL4 an die NOTCH1/4 Rezeptoren führt zur Abspaltung der NOTCH intrazellulären Domäne (NICD) des Rezeptors. Die NICD wandert in den Zellkern und aktiviert dort zusammen im Komplex mit dem Transkriptionsfaktor RBP-JК die Gene HEY1, HEY2 und NRP1. Die Transkriptionsfaktoren HEY1 und HEY2 reprimieren über einen Feedback-Mechanismus direkt die Aktivität des COUP-TFII Promotors.
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Gramm, Stefan. "Thermisch schaltbare Hydrogele - Synthese - Charakterisierung - Anwendung." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2006. http://nbn-resolving.de/urn:nbn:de:swb:14-1163522282581-78351.
Повний текст джерелаАнотація:
Gegenstand dieser Arbeit war die Synthese von thermisch schaltbaren Kammcopolymeren auf Basis von N-(Isopropylacrylamid) (NiPAAm) und Polyethylenglykolmakromonomeren (PEGMA). Die intensive Charakterisierung der aus diesen Copolymeren hergestellten Schichten und deren Anwendung als Zellkultursubstrate war ein weiteres Forschungsziel dieser Arbeit. Die mit Hilfe der neuartigen Schichten erhaltenen Zellkultursubstrate wurden anhand verschiedener adhärenter Zelllinien erfolgreich getestet. Alle getesten Zelltypen (Mausfibroblasten, humane Endothelzellen der Nabelschnurvene und humane korneale Endothelzellen) proliferierten auf den angebotenen Zellkultursubstraten bei 37°C und konnten durch senken der Temperatur geerntet werden.
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Clements, Alice Faith, and alice clements@rmit edu au. "Let's talk (discreetly) about sex. The content generation and design of an online sexual and reproductive health information resource for young Vietnamese: a communications perspective." RMIT University. Applied Communication, 2007. http://adt.lib.rmit.edu.au/adt/public/adt-VIT20080207.100012.
Повний текст джерелаАнотація:
Vietnam is a populous nation experiencing rapid social and economic transition. These changes, in combination with the spread of sexually transmitted infections such as HIV/AIDS, are compromising the reproductive health of young Vietnamese. Access to reliable reproductive health information is limited and social taboos prevent young people from talking openly about this topic. A huge number of young people living in Vietnam thus find themselves without access to relevant, accurate, non-threatening and unbiased information about sexuality and sexual health. The research outlined in this thesis approaches the issue of sexual health information provision for young people living in Vietnam from a participatory action research foundation. A key focus is investigation of the ways in which young people living in Vietnam can be included in the development of online sexual health communication tools by, for and about young Vietnamese. As part of this investigation, this thesis describes research conducted with young Vietnamese in Australia and Vietnam to identify and elucidate their reproductive health information needs, as situated within the contemporary Vietnamese socio-cultural context. The research was undertaken in order to determine how an online resource might meet these needs. This exploratory process involved the utilisation of a range of research methods to determine the website's optimal content, style, features and tone in relation to the Vietnamese context and requirements of its target users. It is hoped that the record of discovery resulting from this research journey will contribute to the existing body of knowledge on online health communication and participatory approaches to the development of context-sensitive health and behaviour-change communication.
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Zaum, Sebastian. "Die hCMEC/D3-Zelllinie als humanes in-vitro-Modell der Blut-Hirn-Schranke im ischämischen Schlaganfall." Doctoral thesis, 2018. https://nbn-resolving.org/urn:nbn:de:bvb:20-opus-166499.
Повний текст джерелаАнотація:
Der Schlaganfall ist eine Krankheit mit großer Bedeutung, sowohl für die Betroffenen wie auch unter volkswirtschaftlichen Gesichtspunkten. In der Erforschung neuer und besserer Therapiemethoden für den ischämischen Schlaganfall ist ein gutes in-vitro-Modell der Blut-Hirn-Schranke unerlässlich, da ein Teil der Schädigung des ZNS durch einen Zusammenbruch dieser Barriere verursacht wird. Die hCMEC/D3-Zelllinie stellt ein solches Modell dar; mit steigender Dauer der ischämischen Stoffwechsellage zeigt sich eine Erhöhung der LDH-Konzentration als Marker für das Absterben der Zellen sowie ein Rückgang der Zellvitalität. Zudem lässt sich eine Entzündungsreaktion mit Anstieg der Marker TNF-Alpha und VEGF, sowie tendenziell auch von Interleukin 6 und Interleukin 8 beobachten, welche auch auf eine Barriereschwächung hindeutet. Aus vorherigen Versuchen bekannte Tight junctions-Proteine wie Claudin 1 und Occludin waren in D3-Zellen unter ischämischen Bedingungen nicht verändert, Claudin 5 war in der PCR vermindert exprimiert. Die für die Barriereschwächung verantwortlichen Strukturproteine müssen durch weitere Versuche identifiziert werden. Eine mögliche Erhöhung der Expression des Transkriptionsfaktors ZO-1 könnte unter diesen Bedingungen einen Mechanismus der Barriereschwächung darstellen. Die Expression des Glukokortikoidrezeptors war in Monokultur-Versuchen mit D3-Zellen nach Ischämie erniedrigt. Dies stellt eine Gemeinsamkeit mit Versuchen mit Zelllinien tierischen Ursprungs dar; in diesen zeigten die Zellen durch Degradation des Glukokortikoidrezeptors ein fehlendes Ansprechen auf eine Glukokortikoid-Behandlung. In der Cokultur der D3-Zellen mit Gliomzellen der C6-Zelllinie zeigte sich jedoch eine Erhöhung der GR-Expression. Eine Cokultur kann den komplexen Aufbau der Blut-Hirn-Schranke, mit Beteiligung mehrerer Zelltypen, besser darstellen als Versuche mit nur einer Zelllinie. Die Erhöhung der GR-Expression in diesem humanen in-vitro-Modell der Blut-Hirn-Schranke steht im Gegensatz zu den in-vitro-Versuchen mit anderen Zelllinien. Dies könnte eine mögliche Erklärung liefern, warum die Erkenntnisse aus diesen Versuchen bisher nicht zu einer Verbesserung der Evidenz der Glukokortikoid-Therapie beim ischämischen Schlaganfall beigetragen haben. Zudem zeigt die Fluoreszenzfärbung von D3-Zellen, dass diese auch unter Ischämie auf Glukokortikoide reagierenThe hCMEC/D3 cell line as human in-vitro-model of the blood brain barrier in ischemic stroke
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Lu, Yung-Feng, and 盧永豐. "A Self-Organizing HCMAC neural network Classifier." Thesis, 2000. http://ndltd.ncl.edu.tw/handle/84315778717111701771.
Повний текст джерелаАнотація:
碩士國立臺灣科技大學
電子工程系
88
A self-organizing HCMAC (Hierarchical Cerebellar Model Arithmetic Computer) neural network classifier which contains a self-organizing input space module and hierarchical CMAC neural network is presented in this thesis. The conventional CMAC can be viewed as kind of basis function networks (BFN) and is useful in two aspects: one is its fast learning speed, and the other is it has a good local generalization capability for approximating nonlinear functions. However, the conventional CMAC needs huge memory requirement, and its performance is highly depended on the approach of input space quantization. To solve these problems, we proposed the self-organizing input space module, which uses Shannon entropy measure to determine adaptive resolutions for all input spaces. Moreover, a hierarchical neural network module was also proposed such that the enormous memory size problem in the conventional CMAC while resolving high dimensional problems can be overcame. Experiments confirm that the self-organizing HCMAC indeed achieve high learning speed and lower memory requirement. Besides, we find that the self-organizing HCMAC classifier has good classification ability by comparing with some other kinds of classifiers.
Книги з теми "HCMEC"
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Bảo tàng mỹ thuật Thành phố Hồ Chí Minh. Mỹ thuật hiện đại Việt Nam: Sưu tập của Bảo tàng mỹ thuật Thành phố Hồ Chí Minh = Vietnamese contemporary art : a collection of HCMC Fine Arts Museum. [Hà Nội]: Nhà xuất bản Mỹ thuật, 2010.
Знайти повний текст джерелаЧастини книг з теми "HCMEC"
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Goldbrunner, Roland H., Martin Bendszus, and Jörg-Christian Tonn. "Protocol for Isolation of HCEC." In Cancer Treatment and Research, 137–38. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4419-8871-3_7.
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Eckert, Ronald, and Le Hai Chau Huynh. "Climate Responsive Neighbourhoods for HCMC: Compact City vs. Urban Landscape." In Sustainable Ho Chi Minh City: Climate Policies for Emerging Mega Cities, 207–38. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-04615-0_12.
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Nguyen, Thi Thanh Huong. "Bus signal priority by active signal program – A case study in Ho Chi Minh City (HCMC), Vietnam." In Lecture Notes in Civil Engineering, 971–76. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-15-0802-8_155.
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Vu, Anh Tuan, and Thi Thanh Huong Nguyen. "Travel behavior change patterns under adverse weather conditions - A case study from Ho Chi Minh City (HCMC), Vietnam." In Lecture Notes in Civil Engineering, 921–26. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-15-0802-8_147.
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Nguyen, Van Tung, Thi Hong Na Le, Hung Tien Le, and Phan Bao Long Nguyen. "An Adaptive Facade Configuration for Daylighting Toward Energy-Efficient: Case Study on High-Rise Office Building in HCMC." In Lecture Notes in Civil Engineering, 39–47. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-3303-5_3.
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Van Ho, Hoa, Truong-Huy Nguyen, Loc Huu Ho, Quang Nguyen Xuan Chau, Linh Ngoc Trinh, and Joong Hoon Kim. "Upgrading Urban Drainage Systems for Extreme Rainfall Events Using Multi-objective Optimization: Case Study of Tan Hoa-Lo Gom Drainage Catchment, HCMC, Vietnam." In Proceedings of 7th International Conference on Harmony Search, Soft Computing and Applications, 51–61. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-2948-9_6.
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Tuan, Vu Anh, and Nguyen Thi Thanh Huong. "Analysis of Mode Choice Behavior under Adverse Weather Conditions Using RA and SA Surveys - A Case Study from Ho Chi Minh City (HCMC), Vietnam." In Lecture Notes in Civil Engineering, 959–64. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-15-0802-8_153.
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Van, Ngo Dau, Phuong Nguyen Kim, Thong Ho Chi, and Thuy Nguyen Thi Ngoc. "Research on Forecasting the Effect of Sea Level Rise on the Riverbed Eccretion and Erosion Process in Sai Gon – Dong Nai River System, HCMC Area." In Lecture Notes in Civil Engineering, 1345–51. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-15-2184-3_176.
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"HCAEC." In Encyclopedia of Cancer, 1635. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_2587.
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Storch, Harry, Ronald Eckert, Nigel Downes, Frank Schwartze, and Chau Huynh. "HCMC: Climate-adapted Planning." In Space, Planning, and Design, 178–91. De Gruyter, 2021. http://dx.doi.org/10.1515/9783868598810-016.
Повний текст джерелаТези доповідей конференцій з теми "HCMEC"
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Sun, Jifeng, Fan Liao, and Yao Peng. "A Clustering Routing Protocol Based on HCMC in WSNs." In 2008 ISECS International Colloquium on Computing, Communication, Control, and Management. IEEE, 2008. http://dx.doi.org/10.1109/cccm.2008.257.
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White, Stephen, Sandro Satta, Georgina Hazell, Jack Teasdale, Graciela Sala-Newby, Tom Johnson, Jason Johnson, Andrew Newby, and Yvonne Alexander. "134 Osgin1 and osgin2 regulate adhesion of HCAEC and potentially contribute to endothelial erosion overlying stenotic plaques." In British Cardiovascular Society Annual Conference ‘High Performing Teams’, 4–6 June 2018, Manchester, UK. BMJ Publishing Group Ltd and British Cardiovascular Society, 2018. http://dx.doi.org/10.1136/heartjnl-2018-bcs.131.
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Mazumdar, Tapati, Akwasi Agyeman, Jerry W. Shay, and Janet A. Houghton. "Abstract 467: New molecular model identifying the critical role of the GLI2 oncogene in human colonic epithelial cell (HCEC) transformation." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-467.
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Dharani, L. R., and S. B. Haug. "Transverse Fracture Toughness of Unidirectional Continuous Fiber and Hybrid Ceramic Matrix Composites." In ASME 1998 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1998. http://dx.doi.org/10.1115/imece1998-1158.
Повний текст джерелаАнотація:
Abstract Reinforcing ceramic materials with unidirectionally aligned continuous fibers improves the mechanical characteristics in the fiber direction but often results in reduced transverse strength and fracture toughness. As an effort to improve the transverse properties of unidirectional fiber reinforecd ceramic matrix composites (FCMC), randomly dispersed fine whiskers can be added to the matrix. The result is a hybrid ceramic matrix composite (HCMC). The objective of this investigation was to ascertain what improvement, if any, can be made through the process of hybridization. The constituent materials evaluated in this study include cordierite (magnesia-alumino-silicate) for the matrix, silicon carbide continuous fiber tow and silicon carbide whiskers. Specimens were fabricated using filament/slurry winding followed by hot press sintering. The specimen bar lengths ranged from 30 to 35 millimeters and had nominally square cross-sections of 4 millimeters. Three-point chevron-notched flexural testing was performed using an MTS-810 servo-hydraulic system. The method presented is based on that which was provided by S-X Wu in ASTM STP 855. The difference here is that a numerical solution is used instead of calibrating fitted stress intensity coefficient curves to the geometry of a material with a well established fracture toughness. The primary advantage to using the cheveron notch profile is that the high stress concentration at the tip of the cheveron ligament induces crack initiation at low loads. As the crack progresses into the increasingly wider portion of the chevron it experiences a decreasing stress intensity field and grows in a stabile fashion as the load is increased. A second advantage is that the stress intensity as a function of crack length is well defined and reaches a minimum at the critical crack length. The need for pre-cracking and the knowledge of the critical crack length are thus avoided. The plane strain opening mode fracture toughness can be determined from specimen geometry, maximum load and flexural span alone. The results from testing confirmed the chevron-notched three-point-bend test produced limited but stable crack growth prior to failure without the introduction of a starting precrack. Instant failure due to crack initiation overload and the resulting potential over-estimate of the transverse plane strain opening mode fracture toughness was avoided. The method presented successfully reproduced the results obtain using other means. The fracture toughness of monolithic cordierite was found to be within 1% of the value published in the Ceramic Source, v8. Substantial improvement to the transverse fracture toughness of a continuous fiber reinforced ceramic matrix composite through the introduction of whiskers to the matrix was demonstrated. When compared with FCMCs with the same base matrix and approximately the same volume fraction of fibers, the HCMCs evaluated in this study displayed a 99% increase in fracture toughness for a crack propagating along the fiber direction and an 82% increase for a crack propagating across the fibers. A significantly greater amount of damage was observed on the fracture surface of the hybrid composite. This indicates more crack deflection and branching due to the presence of the whiskers occurred in the hybrid during fracture. The transverse fracture toughness that results from a crack progressing along the fiber direction was considerably higher than that resulting from a crack propagating across the fiber. More broken fibers were seen on the fracture surfaces of the former. The energy required to break fibers and peal fibers away from the matrix may be responsible for the greater fracture toughness found for a crack propagating in the plane along the fiber direction. Improved load transfer provided by the whiskers in the matrix may aid in the resistance to fiber pealing.
Звіти організацій з теми "HCMEC"
1
Ayallo, Irene. Thesis Review: Evaluating the Impact of Social Change Catalyst on Urban Community Development: A Case Study of LIN Centre for Community Development in Ho Chi Minh City, Vietnam by Chau Doan-Bao. Unitec ePress, June 2018. http://dx.doi.org/10.34074/thes.revw22018.
Повний текст джерелаАнотація:
In this thesis, the author evaluates the impact of the Listen – Inspire – Nurture (LIN) Center’s model of participatory urban community development in Ho Chi Minh City (HCMC). It evidences how LIN has supported urban not-for-profit organisations (NPOs) to alter their self-perception from ‘charity organisations’ to being part of community development processes. Using a participatory communication approach, LIN has encouraged dialogue with and among stakeholders and provided robust information to the community. Consequently, NPOs have become more confident in their own capacities and have more stable financial support. In addition, the corporate sector has a better understanding of the not-for-profit sector and is making a stronger contribution to the development of NPOs in HCMC. These outcomes contribute to effective and sustainable community development in HCMC.
2
Ayallo, Irene. Thesis Review: Evaluating the Impact of Social Change Catalyst on Urban Community Development: A Case Study of LIN Centre for Community Development in Ho Chi Minh City, Vietnam by Chau Doan-Bao. Unitec ePress, June 2018. http://dx.doi.org/10.34074/thes.revw4300.
Повний текст джерелаАнотація:
In this thesis, the author evaluates the impact of the Listen – Inspire – Nurture (LIN) Center’s model of participatory urban community development in Ho Chi Minh City (HCMC). It evidences how LIN has supported urban not-for-profit organisations (NPOs) to alter their self-perception from ‘charity organisations’ to being part of community development processes. Using a participatory communication approach, LIN has encouraged dialogue with and among stakeholders and provided robust information to the community. Consequently, NPOs have become more confident in their own capacities and have more stable financial support. In addition, the corporate sector has a better understanding of the not-for-profit sector and is making a stronger contribution to the development of NPOs in HCMC. These outcomes contribute to effective and sustainable community development in HCMC.